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. 2014 Jun 11;8:153. doi: 10.3389/fnins.2014.00153

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Copyright © 2014 O'Reilly, Kao, Lee and Fenton.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential circuit modifications to attenuate cognitive deficits. One hypothesized cause of cognitive deficits is an imbalance between the entorhinal cortex and CA3 inputs to CA1 that may carry perceptual and memory related information, respectively. Cognitive training may induce synaptic restructuring, for example by increasing the CA3 input and decreasing the entorhinal input to normalize CA1 responses. A second hypothesized cause of cognitive deficits is the abnormal pattern separation computation that might underlie cognitive flexibility deficits. Cognitive training may increase the survival:death ratio of newly born neurons in the dentate gyrus to promote better pattern separation. The adolescent brain may be more receptive to these changes than the adult brain because juvenile brains are actively undergoing similar modifications. CA1, cornu ammonis 1 subregion; CA3, cornu ammonis 3 subregion; DG, dentate gyrus; SUB, subiculum; EC, entorhinal cortex.